NEUROLOGIE Pubmed artikelen Beriberi after bariatric surgery. Goselink RJ, Harlaar JJ, Vermeij FH, Biter UL, Mannaerts GHH, den Heijer T Ned Tijdschr Geneeskd. 2012; 155(23):A4500. Pubmed; 22727224. Bariatric surgery is in general the only effective treatment for morbid obesity. Bariatric surgery is frequently associated with vitamin and mineral deficiencies which may lead to neurological and other symptoms. We describe a case of severe vitamin B1 (thiamine) deficiency. CASE DESCRIPTION: A 49-year-old man visited the emergency department with acute confusion, muscle weakness in arms and legs and visual impairment after a period of dysphagia and recurrent vomiting. Four months earlier, he had had bariatric gastric sleeve surgery for morbid obesity. Laboratory tests demonstrated that he had vitamin B1 deficiency, in view of which the diagnosis of beriberi and Wernicke encephalopathy was made. Despite normalisation of the vitamin B1 concentration following intravenous supplementation, the muscle strength hardly recovered and the patient developed Korsakov syndrome. CONCLUSION: For this deficiency there is no other treatment than vitamin B1 supplementation. Timely recognition of vitamin deficiencies and pro-active supplementation are essential in order to prevent serious complications following bariatric surgery. Common variants at 12q14 and 12q24 are associated with hippocampal volume. Bis JC, DeCarli C, Smith AV, den Heijer T (et al)CHARGE Consortium. Nat Genet 2012; 44:545-552. PMID: 22504421. Free PMC Article. Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer’s disease and vascular risk factors. Our genome-wide association study (GWAS) of dementia-free persons (n = 9,232) identified 46 SNPs at four loci with P values of <4.0 × 10(-7). In two additional samples (n = 2,318), associations were replicated at 12q14 within MSRB3-WIF1 (discovery and replication; rs17178006; P = 5.3 × 10(-11)) and at 12q24 near HRK-FBXW8 (rs7294919; P = 2.9 × 10(-11)). Remaining associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 × 10(-7)) and nine SNPs at 9p33 within ASTN2 (rs7852872; P = 1.0 × 10(-7)); along with the chromosome 12 associations, these loci were also associated with hippocampal volume (P < 0.05) in a third younger, more heterogeneous sample (n = 7,794). The SNP in ASTN2 also showed suggestive association with decline in cognition in a largely independent sample (n = 1,563). These associations implicate genes related to apoptosis (HRK), development (WIF1), oxidative stress (MSR3B), ubiquitination (FBXW8) and neuronal migration (ASTN2), as well as enzymes targeted by new diabetes medications (DPP4), indicating new genetic influences on hippocampal size and possibly the risk of cognitive decline and dementia. 69 WETENSCHAPPELIJK jaarverslag 2012 Pagina 68
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